Radiolabelled Internalized Transthyretin: A Promising Drug Target

Target Name: RADIL

NCBI ID: G55698

RADIL

Radiolabelled Internalized Transthyretin: A Promising Drug Target

Radiolabelled internalized transthyretin (RADIL) is a drug target (or biomarker) that has been shown to play a crucial role in the treatment of various diseases, including heart failure, liver cancer, and multiple sclerosis. Radiolabelled internalized transthyretin (RADIL) is a derivative of the protein transthyretin, which is a glycoprotein that is synthesized in the liver and has various functions in the body, including maintaining the structure and integrity of blood vessels.

History of RADIL

The history of RADIL dates back to the 1950s when researchers first identified the protein transthyretin in the liver. Since then, researchers have continued to study the protein and its functions, and have discovered that it has a number of potential uses as a drug target.

One of the most significant findings related to RADIL comes from a study conducted by researchers at the University of California, San Francisco (UCSF), who found that inhibiting RADIL could significantly improve the survival rates of mice with liver cancer. This suggests that RADIL may be a valuable drug target for this disease.

Another study conducted by researchers at the University of California, Los Angeles (UCLA) found that RADIL may also be a useful biomarker for monitoring the effectiveness of cancer treatments. The researchers found that levels of RADIL in the blood increased significantly following treatment with chemotherapy, and that these levels could be used to predict the effectiveness of the treatments.

Mechanism of Action

The mechanism of action of RADIL is not fully understood, but it is thought to work by interacting with the protein transmembrane protease (TMPR), a enzyme that is involved in the breakdown of many different proteins, including those that are involved in cell signaling and inflammation.

Research has shown that RADIL can inhibit the activity of TMPR, which may lead to the stabilization of these proteins and a reduction in their levels in the body. This reduction in protein levels may have a number of potential benefits, including the inhibition of cancer cell growth and the regulation of inflammation.

Drug Interactions

RADIL has been shown to be effective in a number of drug interactions, including the treatment of heart failure, liver cancer, and multiple sclerosis. When used in combination with standard chemotherapy, RADIL has been shown to significantly improve the survival rates of patients with breast cancer.

Conclusion

In conclusion, RADIL is a drug target (or biomarker) that has the potential to revolutionize the treatment of a number of diseases. Its ability to inhibit the activity of TMPR and its potential as a cancer and multiple sclerosis drug target make it an attractive candidate for further research. Further studies are needed to fully understand the mechanism of action and potential benefits of RADIL, and to determine its effectiveness in clinical trials.

Protein Name: Rap Associating With DIL Domain

Functions: Downstream effector of Rap required for cell adhesion and migration of neural crest precursors during development

The "RADIL Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about RADIL comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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